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Phase 2a > ICS > Flashcards

ICS Flashcards

1
Q

What cells predominate in acute inflammation?

A

Neutrophil polymorphs.

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2
Q

What cells predominate in chronic inflammation?

A

Lymphocytes, plasma cells + macrophages.

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3
Q

Briefly explain the process of acute inflammation.

A
  • Initial reaction of tissue to injury.
  • Vascular component – vasodilation.
  • Exudative component (vascular leakage of protein-rich fluid).
  • Neutrophil polymorph recruitment to tissue.
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4
Q

What are the cardinal features of inflammation?

A
  • Redness (rubor).
  • Het (calor).
  • Swelling (tumor).
  • Pain (dolor).
  • Loss of function.
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5
Q

What are the potential outcomes of inflammation?

A
  • Resolution.
  • Suppuration = pus formaiton.
  • Organisation = repair of specialised tissues by formation of fibrous scar.
  • Chronic inflammation > fibrosis.
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6
Q

What is a granuloma?

A

Aggregate of epithelioid histiocytes.

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7
Q

What is granulation tissue?

A

New connective tissue + small blood vessels that form on surface of a wound.

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8
Q

What is the different between resolution and repair in inflammation?

A
  • Resolution occurs when initiating factor is removed + tissue is either undamaged or able to regenerate.
  • Repair occurs when initiating factor is still present but tissue is damaged/unable to regenerate, involves replacement of damaged tissue by fibrous tissue.
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9
Q

What cells are capable of regeneration?

A
  • Hepatocytes.
  • Pneumocytes.
  • Gut + skin epithelial cells.
  • All blood cells.
  • Osteocytes.
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10
Q

What cells are incapable of regeneration?

A
  • Neurones.

- Myocardial cells.

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11
Q

Define and give an example of…

i) Apoptosis.
ii) Necrosis.
iii) Atrophy.

A

i) Programmed cell death as a result of stimuli, too much = HIV, not enough = cancer.
ii) Traumatic cell death, occurs due to infarction like MI, CVA, frostbite.
iii) Decrease in the size of a tissue caused by a decrease in the number of constituent cells/decrease in their size, seen in Alzheimer’s disease.

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12
Q

Define and give an example of…

i) Hypertrophy.
ii) Hyperplasia.
iii) Metaplasia.

A

i) Increase in size of a tissue caused by an increase in size of constituent cells, building muscle.
ii) Increase in size of a tissue caused by an increase in the number of constituent cells, prostatic hyperplasia.
iii) Change in differentiation of a cell from one fully-differentiated type to a different fully-differentiated type, Barrett’s oesophagus.

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13
Q

Define.

i) Dysplasia.
ii) Neoplasia

A

i) Morphological changes seen in cells progressing to cancer.
ii) New + abnormal growth of tissue in the body which persists despite removal of initial stimulus.

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14
Q

What is a tumour? What’s the difference between benign + malignant neoplasms?

A
  • Any abnormal swelling.
  • Benign = localised, slow growth rate, low mitotic activity.
  • Malignant = invasive, metastases, rapid growth rate.
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15
Q

What are the two types of benign epithelial neoplasms?

A
  • Papilloma = benign tumour of non-glandular, non-secretory epithelium.
  • Adenoma = benign tumour of glandular or secretory epithelium.
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16
Q

What are the two types of malignant epithelial neoplasms?

A
  • Carcinoma = malignant epithelial neoplasm.

- Adenocarcinoma = carcinoma of glandular epithelium.

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17
Q

How are benign connective tissue neoplasms named?

A

Suffix -oma…

  • Rhabdomyoma (striated muscle)
  • Leiomyoma (smooth muscle).
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18
Q

How are malignant connective tissue neoplasms named?

A

Suffix -sarcoma…

  • Liposarcoma = adipose tissue.
  • Angiosarcoma = blood vessels.
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19
Q

What is carcinogenesis?

A
  • Transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations.
20
Q

What type of cancers are caused by…

i) Polycyclic aromatic hydrocarbons (smoking, mineral oils).
ii) Aromatic amines (rubber/dye workers)
iii) Nitrosamines.
iv) Alkylating agents.

A

i) Lung, skin.
ii) Bladder.
iii) Gut.
iv) Leukaemia.

21
Q

How can tumours spread?

A
  • Invades basement membrane using collagenases
  • Tumour motility.
  • Enters lymph/blood vessels.
  • Evades host immune defence.
  • Triggers angiogenesis to nurture growth at new site.
22
Q

What is the likely origin of…

i) Lung metastases?
ii) Liver metastases?
iii) Bone metastases?

A

i) Sarcomas, many common (breast).
ii) Colorectal, stomach, pancreas, carcinoid of intestine.
iii) Prostate, breast, thyroid, lung + kidney.

23
Q

What is innate immunity?

A
  • Non-specific, instinctive, present from birth + first line of defence.
24
Q

Name some components of the innate immune system.

A

Physical + chemical barriers…
- Mucous in resp tract, skin as physical barrier, low vaginal pH, acidic gut.
Phagocytic cells like neutrophils + macrophages.
Serum proteins like complement, acute phase proteins.

25
Q

What ways can complement activation occur?

A 
Classical pathway...
- Antibody-antigen immune complexes.
Alternative pathway...
- Foreign surfaces-antigens.
Lectin pathway...
- Mannose-binding lectin, mannose residues on pathogen surface.
26
Q

What is the complement pathway?

A
  • Lyse microbes directly (formation of membrane attack complex).
  • Increase chemotaxis, cell recruitment (C3a + C5a).
  • Opsonisation (increasing phagocytosis, C3b).
27
Q

What is adaptive immunity?

A
  • Specific, requires lymphocytes, memory + quicker response.
28
Q

What is the major histocompatibility complex? What are the two classes?

A

Proteins that mark a cell as SELF.
Class I = all nucleated cells (not RBCs)
- E.g. virus infected or cancer cell.
Class II = certain immune cells, antigen-presenting.
- E.g. macrophages, B cells, dendritic cells.

29
Q

What are pattern recognition receptors?

A
  • Secreted + circulating like lectins and collectins.

- Cell associated like toll/nod-like receptors.

30
Q

What are the things are recognised in relation to pattern recognition receptors?

A
  • Pathogen associated molecular patterns (PAMPs) like lipopolysaccharides.
  • Damage associated molecular patterns (DAMPs).
31
Q

Where are T lymphocytes produced + matured? How do T cells recognise antigens?

A
  • Produced in bone marrow, mature in thymus.

- Must be displayed by an antigen presenting cell bound to MHC1/2.

32
Q

What are the two types of T cells?

A

Cytotoxic T cells (CD8)…
- Destroy infected body cells (apoptosis) by binding to antigens.
- Binds to MHCI.
T helper cells (CD4)…
- Binds to MHCII.
- Th1 secretes cytokines.
- Th2 activates eosinophils, basophils, induce B cells to make antibodies by releasing cytokines to induce B-cell proliferation.

33
Q

Where are B lymphocytes produced + matured? What do they do? How are they activated?

A
  • Produced + mature in bone marrow.
  • Recognise soluble, free, native, polypeptide antigens.
  • Travel to lymph nodes where they proliferate + differentiate into plasma cells (secrete antibodies) + memory B cells (immunity).
34
Q

What are the functions of antibodies?

A
  • Neutralise toxins.
  • Opsonisation.
  • Activate classical complement system.
35
Q

What are the different types of antibodies?

A
  • IgM = made first.
  • IgG = most common, crosses placenta (passive immunity).
  • IgA = secreted from mucous membranes (breast milk).
  • IgD = B cella ctivation.
  • IgE = histamine reactions + allergies.
36
Q

What is the Fab and Fc region of antibodies?

A
  • Fab region is part that binds to epitope of an antigen.

- Fc region is part that binds to B cells.

37
Q

What does specific binding of the Fab region lead to?

A
  • Neutralise toxins (IgG, A).
  • Immobilise motile microbes (IgM).
  • Prevent binding to + infection of host cells.
38
Q

What are the enhance innate mechanisms with the Fc region?

A
  • Activate complement (IgG, M).
    Bind Fc receptors…
  • Phagocytes (IgG, A) enhances phagocytosis.
  • Mast cells (IgE) release inflammatory mediators.
  • Natural killer cells (IgG) enhanced killing of infected cells.
39
Q

What is hypersensitivity?

A
  • The immune system responds inappropriately to a normal harmless antigen.
40
Q

What is a type 1 hypersensitivity reaction

A
  • IgE mediated, allergic + acute.
  • IgE binds to mast cells causing histamine release.
  • Anaphylaxis, hayfever.
41
Q

What is a type 2 hypersensitivity reaction

A
  • IgG bound to cell surface antigens/IgM

- Transfusion reactions, autoimmune disease, goodpastures.

42
Q

What is a type 3 hypersensitivity reaction

A

Immune complexes, activation of complement/IgG.

- SLE.

43
Q

What is a type 4 hypersensitivity reaction

A

T-cell mediated delayed type hypersensitivity.

- TB, contact dermatitis.

44
Q

Briefly describe immunity.

A

First exposure…
- IgM made first, rapidly increases.
- IgG begins to be made, rapidly increase.
- IgM decreases first, IgG decreases after.
Second exposure…
- IgG RAPIDLY produced in vast quantities.
- Small rise in IgM.
- Symptoms not experienced second exposure.

45
Q

What is the aim of vaccinations?

A
  • Achieve long-term protection, stimulate both B+T cells, induce memory B+T cells + stimulate protective high affinity IgG production.

Phase 2a (12 decks)

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